Authors
Alessandro Venturino, MohammadAmin Alamalhoda, Thomas Negrello, Kelly Jin, Cindy T J van Velthoven, Ryan John A Cubero, Jake Yeung, Peter Koppensteiner, Bosiljka Tasic, Sandra Siegert
Published in
Science advances. Volume 12. Issue 31. Pages eadz6517. Jul 31, 2026. Epub Jul 31, 2026.
Abstract
Anesthesia recovery is critical for resuming normal physiological and neuronal functions; however, the mechanisms involved remain elusive. Here, we identify a female-selective corticosterone-mediated microglia-neuron interaction during ketamine anesthesia recovery, absent in males. This microglia-neuron interaction induces plastic and functional neuronal changes, as evidenced by increased mEPSC frequency, which was occluded upon microglia depletion. We showed that this process is driven through up-regulation of the stress-responsive co-chaperone Fkbp5 mRNA and its protein, Fkbp51, in female microglia. Fkbp5/Fkbp51 is a key intermediary in a corticosteroid-induced stress response, and its involvement points toward a critical interface between endocrine signaling and microglia. To counteract the observed ketamine anesthesia-mediated increase in blood corticosterone during recovery, we removed the primary source of corticosterone by adrenalectomy. Close microglia-neuron interaction was reduced and increased again following corticosterone injection. Our findings identify a sex-specific microglia-mediated mechanism of neuronal plasticity during anesthesia recovery, driven by corticosterone, thereby enhancing our understanding of sex differences in brain function.
PMID:
42536755
Bibliographic data and abstract were imported from PubMed on 01 Aug 2026.
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